Identified serotonergic neurons in the Tritonia swim CPG activate both ionotropic and metabotropic receptors

Although G-protein-coupled (metabotropic) receptors are known to modulate t he production of motor patterns, evidence from the escape swim central patt ern generator (CPG) of the nudibranch mollusk, Tritonia diomedea, suggests that they might also participate in the generation of the motor pattern its elf. The dorsal swim interneurons (DSIs), identified serotonergic neurons i ntrinsic to the Tritonia swim CPG, evoke dual component synaptic potentials onto other CPG neurons and premotor interneurons. Both the fast and slow c omponents were previously shown to be due to serotonin (5-HT) acting at dis tinct postsynaptic receptors. We find that blocking or facilitating metabot ropic receptors in a postsynaptic premotor interneuron differentially affec ts the fast and slow synaptic responses to DSI stimulation. Blocking G-prot ein activation by iontophoretically injecting the GDP-analogue guanosine 5' -O-( 2-thiodiphosphate) (GDP-beta -S) did not significantly affect the DSI- evoked fast excitatory postsynaptic potential (EPSP) but decreased the ampl itude of the slow component more than 50%. Injection of the GTP analogues g uanosine 5'-O-(3-thiotriphosphate) (GTP-gamma -S) and 5'-guanylyl-imidodiph osphate, to prolong G-protein activation, had mixed effects on the fast com ponent but increased the amplitude and duration of the slow component of th e DSI-evoked response and, with repeated DSI stimulation, led to a persiste nt depolarization. These results indicate that the fast component of the bi phasic synaptic potential evoked by a serotonergic CPG neuron onto premotor interneurons is mediated by ionotropic receptors (5-HT-gated ion channels) , whereas the slow component is mediated by G-protein-coupled receptors. A similar synaptic activation of metabotropic receptors might also be found w ithin the CPG itself, where it could exert a direct influence onto motor pa ttern generation.